Alteration in sarcoplasmic reticulum-dependent contraction of tail arteries in response to caffeine and noradrenaline in spontaneously hypertensive rats.

Since the membrane Ca2+ handling properties of the arterial smooth muscle sarcoplasmic reticulum may be altered in genetic hypertension, we studied caffeine- and noradrenaline-induced contractions in tail arteries from spontaneously hypertensive rats (SHR) at the prehypertensive stage (4 weeks old) and from age-matched Wistar-Kyoto rats (WKY). After the sarcoplasmic reticulum had been loaded with Ca2+ by pretreatment with physiological Ca2+ solution, caffeine- and noradrenaline-induced contractions of the tail arteries, measured in a Ca2(+)-free solution [containing 0.1 mmol/l ethyleneglycol-bis-(beta-aminoethylether)-N,N,N',N'-tetraace tic acid], were smaller in SHR than in WKY. After caffeine-releasable Ca2+ in the sarcoplasmic reticulum had been depleted by pretreatment with the Ca2(+)-free solution, the caffeine-induced arterial contractions in a low-Ca2+ (0.5 mmol/l) solution were smaller in SHR than in WKY. The Ca2+ concentration-tension relationship in skinned arterial fibres was similar in WKY and SHR. These data suggest that the ability of the sarcoplasmic reticulum to take up and store caffeine- and noradrenaline-releasable Ca2+ is decreased in SHR. The development of hypertension in SHR may be explained by an impaired function of the sarcoplasmic reticulum in arterial smooth muscle.